The main objective of this proposed research is to elucidate the regulation of the mammalian growth cycle and determine how viral transformation alters that regulation. Normal growth control of fibroblast cells by serum components can be separated into two discrete phases. The first phase, termed competence, is induced by a platelet derived mitogen. Competent cells are potentially able to enter the growth cycle. The second phase of control is termed progression and is controlled by factors present in platelet-poor plasma. Progression involves traverse of the growth cycle. Cells transformed with tumor virus (RNA or DNA) do not require platelet mitogen for growth in medium supplemented with platelet-poor plasma. SV40 infection of BALB/c-3T3 cells abrogates the requirement for platelet mitogen to initiate DNA synthesis and growth. I have proposed to isolate the factors present in plasma that allow cell cycle traverse. The nature of these factors and their mechanism of action can lead to the understanding of the control of cell cycle traverse. I have also proposed the identification of the protein made in response to platelet mitogen and SV40 infection in order to determine if they induce cell growth by the same or different mechanisms. These data will indicate whether or not the transformed abnormal growth state is due to a permanant competence state in the viral-transformed cell.